Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004610 (bacteremia)
 13,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-two cases of Xanthomonas maltophilia bacteremia have been identified over the last two years at the Veterans General Hospital, Taipei. Among them, 27 cases (84%) were due to hospital-acquired infections, and 14 cases (44%) were polymicrobial bacteremia. One case was confirmed as prosthetic valve endocarditis and one case was complicated by recurrent attacks of ecthyma gangrenosum. Most cases had severe debilitating conditions. Twelve cases (38%) had a malignancy, 19 cases (59%) were resident in the Intensive Care Unit and 16 cases (50%) had undergone major surgery. The main predisposing factors included central venous catheterization, endotracheal intubation or tracheostomy, prior antibiotic therapy and prolonged hospitalization. Moxalactam, chloramphenicol and trimethoprim-sulfamethoxazole were the most effective agents in vitro against X. maltophilia. Twenty-two cases (69%) died during hospitalization; 13 cases (41%) were directly attributed to septicemia. Factors that adversely influenced mortality included inappropriate antimicrobial therapy and prior antibiotic treatment. Of particular interest is the fact that none of the patients who did not receive appropriate antimicrobial therapy survived. Early diagnosis and appropriate antibiotic therapy are critical for improving the prognosis of X. maltophilia infection.
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PMID:Xanthomonas maltophilia bacteremia: an analysis of 32 cases. 136 39

To determine the effect of methylprednisolone administration on the clearance of bacteremia and the release and clearance of endotoxin during antibiotic therapy of gram-negative bacterial sepsis, Escherichia coli K1 sepsis was induced in paired rabbits. Moxalactam and either methylprednisolone or placebo were administered to infected rabbits 1.5 h after intraperitoneal administration of live bacteria. Serial blood samples were obtained for quantitation of bacteremia and endotoxemia, arterial blood gases, and complete blood count. Arterial blood pressure, heart rate, and core body temperature were also monitored. There were no significant differences between the methylprednisolone-treated and placebo-treated groups in either the levels of bacteremia or endotoxemia or in the physiologic, metabolic, or hematologic parameters that were measured. We conclude that methylprednisolone administration has no acute effect on bacterial clearance or on the kinetics of endotoxin release and clearance during antibiotic therapy of gram-negative bacterial sepsis in this experimental model.
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PMID:Effect of methylprednisolone on bacterial clearance and endotoxin liberation during experimental sepsis induced by gram-negative bacteria. 395 27

Sixty-seven patients were treated with moxalactam in a noncomparative trial of hospitalized patients; 32 had endometritis or chorioamnionitis, 12 had skin and soft tissue infections, 5 had osteomyelitis, 5 had pneumonia, 5 had urinary tract infections, 4 had arthritis, 2 had sepsis from an unknown source, 1 had endocarditis, and 1 had peritonitis. Bacteremia was present in 12 of these patients. Patients were given 3 to 12 g of moxalactam per day (mean, 6.24 g/day) in divided doses every 6 to 8 h. Seven patients were given intramuscular treatment for 3 to 20 days for part or all of their therapy. The rest were given intravenous treatment exclusively. Treatment was continued for 2 to 42 days (mean, 10 days). The dose and the duration of therapy were determined by the type of infection and the response of each patient. There were four treatment failures and one enterococcal-clostridial superinfection. Moxalactam was well tolerated. Allergic reactions led to the discontinuation of the antibiotic in three patients. Prolonged prothrombin and partial thromboplastin times were observed in 2 of 11 patients tested; in both instances in patients had severe underlying diseases, including malnutrition and alcoholism. Pain on intramuscular injection was noted in two patients receiving 1,500 mg, but not in five receiving a lower dose; in one case the pain forced the use of intravenous therapy after one dose, and in the other case the pain was mild and the patient was treated for 20 days. We concluded that moxalactam was effective in the treatment of the types of infections included in this study and produced few adverse reactions.
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PMID:Moxalactam in the therapy of serious infections. 621 Nov 40

Sixty-five episodes of nosocomial infections of the blood, lungs, urinary tract, soft tissues, bones, or central nervous system were treated with intravenous moxalactam (3-12 g per day). Bacteremia was documented in 21 patients. Despite the severely compromised condition of many patients, 80% of the infections responded satisfactorily, as defined by clinical and microbiologic cure or improvement. Of the 21 cases of nosocomial bacteremia, 14 (67%) responded satisfactorily. Of the six cases of bacteremia caused by gram-negative bacilli resistant to aminoglycosides, three responded satisfactorily. Moxalactam therapy also resulted in cure or improvement in nine (69%) of 13 pulmonary infections, and it was used alone to cure one case of meningitis-ventriculitis due to Klebsiella pneumoniae. Seven of 13 therapeutic failures involved Pseudomonas aeruginosa, and moxalactam-resistant P. aeruginosa emerged during therapy for 12 patients. Adverse effects, usually mild diarrhea, occurred in 9.2% of the patients. Except for some severe infections due to P. aeruginosa, moxalactam is effective and safe therapy for nosocomial infections caused by susceptible organisms.
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PMID:Moxalactam for treatment of nosocomial infections. 621 78

Moxalactam was studied in a prospective randomized clinical trial in 97 hospitalized patients suspected of having infection caused by moxalactam-susceptible bacteria. Seventy-eight of the 97 patients had clinical and/or bacteriologic evidence of infection, including pneumonia, cellulitis, urinary tract infection, bacteremia, and fever in neutropenic patients. Patients in the control group received antibiotics deemed appropriate by the attending physicians, whereas the moxalactam-treated group received only the study drug. Successful treatment was defined as the resolution of illness sufficient to allow discontinuation of parenteral antibiotic therapy. No significant difference was seen in efficacy with 33 (86.8%) of 38 patients in the moxalactam-treated group and 32 (80%) of 40 in the control group treated successfully (P greater than 0.20). The mean number of febrile days was significantly less in the moxalactam-treated group than in the control group (P less than 0.05). Renal toxicity occurred more frequently in the control group (P = 0.036). Fungal superinfection developed in two patients in the control group and in one in the moxalactam-treated group. An enterococcal superinfection of the bloodstream developed in one patient treated with moxalactam. Thus moxalactam appears to be comparable in efficacy to combinations of antibiotics in the treatment of selected seriously ill patients and may have less renal toxicity.
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PMID:Moxalactam therapy vs. standard antimicrobial therapy for selected serious infections. 621 77

Bacterial peritonitis, intraabdominal sepsis, and other surgical infections are frequently polymicrobial. Moxalactam, a new beta-lactam antibiotic, has been shown to be active in vitro against most bacterial pathogens commonly isolated from patients with surgical infections. This drug was therefore tested as the sole antimicrobial agent in the treatment of 32 surgical infections (25 cases of intraabdominal sepsis, 6 cases of wound infections, and 1 case of bacteremia). Nearly all (91%) of the infections responded favorably; 66% were cured with moxalactam plus surgery, 16% were cured with moxalactam alone, and 9% improved. Moxalactam-resistant strains of bacteria were isolated from 18 infections but were associated with therapeutic failure in only two cases and with superinfection in three cases. On the basis of these data, we believe that moxalactam is an effective and safe antimicrobial agent for use alone in the treatment of serious intraabdominal infections.
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PMID:Moxalactam in the treatment of intraabdominal sepsis and other surgical infections. 621 82

Moxalactam and the third-generation cephalosporins are ineffective against enterococci in vitro. Therefore, the case reports of 2,107 patients treated with moxalactam for a variety of infections were reviewed for determination of the incidence of superinfection with enterococci. This complication occurred in 2.1% of the cases, most frequently in patients with urinary tract infections and urinary catheters. Seven patients developed enterococcal bacteremia during moxalactam therapy. It was not demonstrated that the presence of enterococci in initial cultures was associated with adverse therapeutic results in patients with skin, soft tissue, intraabdominal, and gynecologic infections.
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PMID:Enterococcal infections in patients treated with moxalactam. 621 88

Moxalactam was used as initial, empirical therapy in 69 patients with a variety of serious bacterial infections, 32% of which were accompanied by bacteremia. Overall, the success rate was 83% and drug-related adverse effects were minimal. The drug was less efficacious in infections caused by aerobic gram-positive pathogens than it was in those caused by gram-negative pathogens. The following gram-positive organisms were associated with special problems during moxalactam therapy: Streptococcus pneumoniae (development of meningitis and a relapse of pneumonia with a more resistant strain), Staphylococcus epidermidis (in vivo emergence of moxalactam resistance, and the enterococci (failure of therapy and a fatal superinfection. Moxalactam performed well in infections caused by most gram-negative organisms, including aminoglycoside-resistant strains, but the previously reported emergence of gram-negative bacillary resistance to moxalactam during therapy was reconfirmed in our series with Serratia marcescens. The use of moxalactam in the treatment of gram-negative meningitis was further supported by a patient with meningitis-ventriculitis caused by Bacteroides fragilis who was cured with moxalactam after failure on chloramphenicol.
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PMID:Clinical evaluation of moxalactam: evidence of decreased efficacy in gram-positive aerobic infections. 622 96

A model of overwhelming E. coli K1 sepsis and early meningitis was developed in infant rabbits and used to compare clinical and bacteriologic efficacy of ampicillin, moxalactam, cephalothin and chloramphenicol. Intraperitoneal injection of 10(7) E. coli K1 into 1- or 2-wk-old rabbits produced a rapidly progressive infection which, if left untreated, produced bacteremia in 100% of animals, meningitis in 78%, and mortality in 100%. Therapy was initiated 4 h after ip infection at which time mean bacterial concentration (log10 CFU/ml) ranged from 4.4-4.8 in the blood and from 1.8-2.3 in the cerebral spinal fluid (CSF). Pre-treatment frequency of bacteremia (100%) and meningitis (17-23%) was similar for all experimental groups. Antibiotic concentrations in blood and CSF 2 h after a dose exceeded the E. coli minimum inhibitory concentration with the exception of CSF cephalothin, which was undetectable. Moxalactam, ampicillin, and chloramphenicol significantly reduced the incidence of bacteremia and meningitis relative to cephalothin or saline controls (P less than 0.02). Mortality rates among the former three groups were high (64-82%) but significantly less than in saline or cephalothin-treated rabbits (100%). In this neonatal model of fulminant sepsis with early meningitis, moxalactam provided no therapeutic advantage over ampicillin or chloramphenicol.
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PMID:Antibiotic therapy of fulminant E. coli K1 sepsis in infant rabbits. 637 94

In a prospective randomized trial, febrile granulocytopenic patients received either moxalactam plus piperacillin or moxalactam plus amikacin as initial empiric antimicrobial therapy. Most patients were also given prophylactic vitamin K. The overall response rates for the two regimens were similar (105 of 136, or 77 percent, for moxalactam plus piperacillin versus 107 of 136, or 79 percent, for moxalactam plus amikacin). For Pseudomonas aeruginosa infections, the response rate was better in patients receiving moxalactam plus amikacin (seven of nine versus one of five, p = 0.06); two patients treated with moxalactam plus piperacillin experienced relapse of P. aeruginosa bacteremia in association with the emergence of beta-lactam-resistant P. aeruginosa isolates. On the other hand, bacteremic enterococcal superinfections occurred in seven patients receiving moxalactam plus amikacin but in none given moxalactam plus piperacillin (p = 0.02). Serious side-effects were minimal with both regimens, and nephrotoxicity was less common in patients receiving moxalactam plus piperacillin (two of 136 versus six of 136, p = 0.28). There was no antibiotic-related hemorrhage. These results suggest that the overall efficacy and toxicity of moxalactam plus piperacillin and moxalactam plus amikacin are similar. Moxalactam/piperacillin therapy may be limited in certain patients by the emergence of beta-lactam-resistant P. aeruginosa, whereas enterococcal superinfections may complicate moxalactam/amikacin therapy.
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PMID:Moxalactam plus piperacillin versus moxalactam plus amikacin in febrile granulocytopenic patients. 647 84


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